Can Inhaled Corticosteroids Slow COPD Lung Function Decline?

June 20, 2020

Inhaled corticosteroids for patients with chronic obstructive pulmonary disease (COPD) may curb lung function decline, according to new research.

Exacerbations in patients with chronic obstructive pulmonary disease with high blood eosinophil count (BEC) may lead to further disease progression, according to a paper published in the journal Thorax.

Investigators from across the globe recruited adult patients from 2 large electronic medical record databases in the United Kingdom and followed them for 3 years in order to determine whether inhaled corticosteroid (ICS) use and BEC affect COPD progression. The patients had a mild to moderate COPD, plus a history of smoking tobacco, but were not included in the analysis if they had a diagnosis of asthma.

The study authors explained that BEC is known to predict both the risk of future exacerbations among patients with COPD and response to ICS in terms of exacerbation prevention and improved lung function. Patients with high BEC have been found to be most responsive to ICS treatment, previous studies have noted. However, it is yet to be determined if BECs are a good biomarker to identify patients who would benefit most from ICS intervention.

About half of the 12,178 patients in the analysis were female with a mean age of 66 years. Three-quarters of the patients received ICS. The study authors had available BEC data from 62% of patients who initiated ICS and 66% of patients who initiated non-ICS therapy as their highest maintenance of therapy. Counts were similar in both groups, they said, though a higher proportion of patients in the ICS therapy group had a high BEC compared to patients in the non-ICS therapy group. For example, in the ICS group, 20% and 11% had BEC of ≥350 and ≥450 cells/µL, respectively, compared to 17% and 7% in the non-ICS group.

A majority of the patients had BEC of 50-349 cells/µL, the authors said, while 3% had <50 and almost 20% had ≥350. The patients with the highest BECs were more frequently male, more often had a previous diagnosis of nasal polyps, and had higher rates of exacerbations, the study authors wrote. The patients in the lowest BEC group had relatively low body mass index, a diagnosis of osteoporosis more often, received more prescriptions for oral corticosteroids, and consulted their general practitioner for reasons outside of COPD more often, they added.

Patients in the highest BEC group had the lowest absolute level of lung function decline, but when these patients experienced exacerbations while not treated with ICS, there was a substantial decline in lung function.

For patients in the middle group, the study authors noted no significant excess lung function decline in relation to increasing exacerbation rates for those who did not receive ICS, but it was present and significantly greater for those treated with ICS.

For patients with BEC <50 cells/µL, the study authors said there was no significant difference between exacerbation rate and excess decline either for patients with or without ICS treatment.

This study also measured lung function against type of treatment. There were 14,572 patients treated with ICS and 4,867 without ICS. Patients with higher annual rates of exacerbations after the start of their ICS therapy had significantly faster decline of FEV1. But they said the rate of decline was similar among those treated with non-ICS.

Finally, the authors found that patients with low level adherence to ICS treatment had significantly more decline than patients with good adherence.

“An individual with repeated exacerbations and a high BEC but not on ICS therapy may be subject to faster lung function decline,” the authors concluded. “ICS-containing therapies in these patients could attenuate lung function decline, but more research is needed to confirm this.”

Reference

Kerkhof M, Voorham J, Dorinsky P, et al. Association between COPD exacerbations and lung function decline during maintenance therapy. Thorax. Published online June 12, 2020. doi:10.1136/thoraxjnl-2019-214457